ALCAR is reported to be a naturally occurring substance that, when used or administered at supraphysiologic concentrations, is neuroprotective in various models of focal cerebral ischemia.
On the other hand, oxidative stress and neuroinflammation are the central factors that cause progressive degeneration of dopaminergic neurons in Parkinson’s disease.
The neural stem cells, on the other hand, underwriters in maintaining brain plasticity; hence, survival of neural stem cells and neuroblast in the process of the neurodegenerative process becomes significant in refilling the puddle of established neural population. And because ALCAR is present in almost all the body cells, it heightens endogenous antioxidants and regulates biogenetics.
In the contemporary medicine and healthcare setting, there is no evidence suggesting the putative mechanism and neuroprotective effects of ALCAR in 6-OHDA induced rat and mode of PD-like phenotypes. In this case, we examined the impact of ALCAR on death/survival of dopaminergic, neuroblast, and NSCs and the associated mechanism of the neuroprotection in 6-OHDA rat of PD-like phenotypes. In the diagnosis process, using ALCAR (100 mg/kg/day, intraperitoneal (i.p.)) treatment began three days earlier to 6-OHDA lessening and proceeded for another fourteen-day post-lessoning (Levy et al., 2009). From the lab result, it was discovered that the pre-treatment of ALCAR in 6-OHDA-lesioned rats increased the expression of the neurogenic and the pathway genes in the striatum and substantia nigra pars compacta (SNpc) region.
Separately, exposure of the cultured neural cells to ALCAR inhibits apoptosis caused by the deprivation of serum. Besides, it was discovered that the pretreatment using ALCAR in 6-OHDA-lesioned reduced GSK-3β stimulation and amplified nuclear translocation of β-catenin. Purposeful deficits were reestablished subsequent ALCAR pretreatment in 6-OHDA-lesioned rats as established by the better-quality motor organization and revolving behavior, authorizing fortification of DAergic innervations in lesioned striatum (Singh et al., 2017). In conclusion, the overall result of the investigation suggests that ALCAR exercises exclusive neuroprotective effects through the stimulation of β-catenin pathway, telling its beneficial use to treat neurodegenerative sicknesses by improving reformative capability and subsequently neuroprotection.References
Levy, O. A., Malagelada, C., & Greene, L. A. (2009). Cell death pathways in Parkinson’s disease: proximal triggers, distal effectors, and final steps. Apoptosis : An International Journal on Programmed Cell Death, 14(4), 478–500. http://doi.org/10.1007/s10495-008-0309-3
Singh, S., Mishra, A., Mishra S, & Shukla, S. (2017). ALCAR promote adult hippocampal neurogenesis by regulating cell-survival and cell death-related signals in rat model of Parkinson’s disease like-phenotypes. 108:388-396. doi: 10.1016/j.neuint
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